Relationship Between T Cell Regulation And Type I Diabetes

Abstract The purpose of this study is to explore the relationships and mechanisms between T-cell regulation and type I diabetes by using NOD mice model. NOD mice can spontaneously develop a form of autoimmune diabetes which is similar to human Insulin-Dependent Diabetes Mellitus. T cells can destroy beta cells of the pancreatic islets which can produce insulin. Thus, by analyzing the development of NOD mice autoimmune diabetes to determine potential treatment for type I diabetes. Introduction Diabetes mellitus is a group of metabolic diseases. There are different kinds of diabetes mellitus, but an abnormal blood sugar level over an extended time always can be detected from patients who have this disease. Type one diabetes mellitus also known as insulin-dependent diabetes, patients with this type of diabetes have pancreatic beta cells destruction causing absolute lack of insulin with a tendency to ketoacidosis. It can occur at any age, but more commonly occurs in young people. Patients with acute onset of metabolic disorders symptoms need insulin injections to survive. This type of diabetes including immune-mediated and idiopathic two subtypes. Immune-mediated diabetes often has one or more autoantibodies present, for example, islet cell antibodies (ICA), insulin autoantibodies (IAA) and glutamic acid decarboxylase 65 (GAD65) antibodies. Previous studies have shown that killer T cells that protects us from bacterial damage plays a major role in theShow MoreRelatedCase Control Study961 Words   |  4 Pagesrs3745453 polymorphism on MS risk in a sample of Isfahan population. We found that miR-23a rs3745453 CT variant seem to increase the risk of MS in this population (OR =2.5). Compared with ridolfi et al. The results did not support an association between rs3745453 allele C polymorphism and MS risk(p-value 0.16). Ridolfi et al. in 2013 reported that levels of miR-15b and miR-23a were decreased in the serum of Multiple Sclerosis patients compared with controls. 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